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Biomedical subjects

S D Kosanke

Publications and source records attributed to S D Kosanke.

30 records · Page 2Linked to original sources
PubMed1981

Disseminated staphylococcal infection in a colony of captive ground squirrels (Citellus lateralis).

Purulent cutaneous and visceral lesions were observed in a colony of 68 golden-mantled ground squirrels, Citellus (Spermophilus) lateralis, used in a hibernation study. The squirrels had been purchased from a commercial supplier. Beginning approximately three weeks after their purchase and during the following five weeks, 21 squirrels died. The predominate gross and histologic findings consisted of multifocal suppurative lesions involving the skin, brain and numerous visceral organs. Staphylococcus aureus was consistently found to be associated with the disease.

Animals↗
PubMed1979

Fatal Beauveria bassiana infection in a captive American alligator.

The entomopathogenic fungus, Beauveria bassiana, was isolated from pulmonary lesions of a dead American alligator (Alligator mississipiensis) at the Oklahoma City Zoo. Colonies of the fungus, which had sporulated in vivo, were found in the thoracic air spaces. Septate, branching hyphae and fungal spores were seen in stained histologic sections of pleura and lung. Dissemination to other viscera had not occurred. This case indicated that B bassiana, a rare vertebrate pathogen, may be a fatal mycotic agent in captive reptiles.

Alligators and Crocodiles↗
PubMed1979

Extracorporeal perfusion without anticoagulation and the response to endotoxin.

The results of this study show that an extracorporeal perfusion system without anticoagulation can be established in the dog under certain conditions. The exact mechanisms merit further investigation. It also points to a model to study the effects of endotoxin without heparin interference and as another model for studying the canine blood coagulation system.

Animals↗
PubMedDate not supplied

Long-term intracoronary ethanol administration electrophysiologic and morphologic effects.

The long-term intracoronary infusion of ethanol was used to evaluate the potential of ethanol to produce myocardial injury and cardiac rhythm disturbances. In 22 dogs, electrophysiologic testing was performed 48 hr after cessation of alcohol administration. Multiple premature ventricular beats occurred spontaneously in 3 dogs with spontaneous sustained monomorphic ventricular tachycardia observed in 1 dog. Provocative ventricular pacing produced ventricular tachycardia lasting 20 or more beats in 13 animals with sustained tachycardia observed in 3 animals. Provocative ventricular pacing in the presence of lidocaine or epinephrine produced sustained ventricular tachycardia in an additional 4 dogs. The electrophysiologic properties of Purkinje fibers from the zone receiving ethanol were altered when compared to the control zone. The resting membrane potential was decreased (-76 +/- 2 mV vs. -85 +/- mV, p less than 0.001) with a decrease in action potential amplitude (91 +/- 4 vs. 109 +/- 2 mV, p less than 0.001) and phase 0 upstroke (231 +/- 27 vs. 456 +/- 25 V/sec, p less than 0.02). Prolonged refractoriness was observed in the ethanol zone without a prolongation of action potential duration. Intramural lesions observed within the left circumflex distribution varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The data suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histologic and electrophysiologic injury in the canine heart. The electrophysiologic ch changes provide a substrate sufficient for the induction and maintenance of ventricular arrhythmia.

Action Potentials↗
PubMedDate not supplied

Redox cycling and hepatotoxicity of diquat in aging male Fischer 344 rats.

The aim of this study was to determine the influence of aging on diquat-induced redox cycling in liver microsomes and diquat hepatotoxicity in rats. Diquat-stimulated production of superoxide anion radical and NADPH-cytochrome c (P-450) reductase activity were measured in liver microsomes prepared from male Fischer 344 rats at ages representing young adulthood (5-6 months), middle age (15-16 months), and old age (24-27 months). Both activities were decreased substantially (40%) in old rats. Diquat-induced liver damage was assessed 6 hr after the administration of diquat (0.1 mmol/kg, ip) on the basis of serum ALT and sorbitol dehydrogenase activities, hepatic microsomal cytochrome P-450 loss, and histological evaluation. The classical manifestations of hepatotoxicity in diquat-treated rats were as severe in old rats as in young-adult ones, despite the age-associated drop in redox cycling capacity. Diquat treatment also resulted in decreased concentrations of hepatic glutathione and ascorbic acid, increased concentrations of hepatic nonheme iron, and decreased liver weights. The changes in glutathione, nonheme iron, and liver weight were more pronounced in livers of middle-aged and old rats than in those of young-adult rats. These age-dependent differences could not be explained on the basis of plasma diquat concentrations, which were similar in the three age groups of rats. The absence of an effect of aging on the hepatotoxic effects of diquat indicates that redox cycling capacity is not limiting for the development of liver damage. Other effects of diquat were influenced by aging, but their relevancy to the hepatotoxicity is uncertain.

Aging↗